UNG (uracil DNA glycosylase) is a base excision repair enzyme that hydrolyzes the N-glycosidic bond between uracil and deoxyribose in DNA, releasing free uracil and generating abasic (AP) sites 1. The UNG gene produces two protein isoforms through alternative splicing: nuclear UNG2 and mitochondrial UNG1, each with distinct subcellular localization 1. UNG2 localizes to replication forks where it removes both misincorporated dUMP residues and uracil from U:G mispairs arising from cytosine deamination, with PCNA and RPA recruiting it to nascent DNA strands 1. UNG functions in two critical biological processes: error-free DNA repair to prevent mutagenesis, and mutagenic uracil processing during antibody diversification 2. In B cells, UNG processes activation-induced cytidine deaminase (AICDA)-induced uracil to facilitate both class switch recombination and somatic hypermutation 2. Notably, UNG can perform intrinsic strand-incision activity, generating 3′-α,β-unsaturated aldehyde products subsequently processed by APE1 3. Mutations in UNG cause immunodeficiency with hyper-IgM 5, characterized by recurrent infections, defective class switching, and elevated IgM with reduced IgG/IgA/IgE 2. Recent evidence demonstrates UNG is essential for APOBEC3-mediated mutagenesis in cancer cells and represents a therapeutic target in BRCA1/2-deficient tumors 4 5.